Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/7686
Title: GADD45? methylation is more common in benign prostatic hyperplasia than in prostate cancer
Authors: Can, O.
Caner, Vildan
Türk, Nilay Şen
Tuncay, Ömer Levent
Eskicorapci, S.Y.
Tepeli, Emre
Çetin, Ozan
Keywords: Benign prostatic hyperplasia
DNA methylation
GADD45?
Prostate cancer
growth arrest and DNA damage inducible protein 45
growth arrest and DNA damage inducible protein 45 gamma
unclassified drug
adult
aged
article
controlled study
high resolution melting analysis
human
human tissue
immunohistochemistry
major clinical study
male
prostate cancer
prostate hypertrophy
protein expression
comparative study
correlational study
epigenetics
GADD45gamma gene
pathogenesis
protein function
regulatory mechanism
Publisher: Gene Therapy and Molecular Biology
Abstract: Prostate cancer (PCa) is one of the most common cancer types worldwide in men. Although Growth Arrest DNA Damage-Inducible 45 (GADD45) family members, GADD45? , GADD45? and GADD45? , are responsible for the activation of several molecules in certain cellular pathways affecting cell fate, including tumorigenesis, as stress sensors, the role of GADD45? in PCa is still not clear. In this study, our aim was to detect the methylation and protein expression profiles of GADD45? in benign prostate hyperplasia (BPH) (60 patients) and PCa (56 patients). The methylation of GADD45? was determined by methylation-sensitive high resolution melting analysis. Immunohistochemistry was used for evaluating GADD45? protein expression. The methylation frequency for GADD45? was as low as 1.8% in PCa compared with BPH (P=0.000). GADD45? protein was overexpressed in PCa cases (53.6%) compared with the BPH cases (33.3%), and the difference was statistically different (P=0.028). There was no correlation between GADD45? methylation and protein expression in both groups. This study shows that in contrast to hematological malignencies, GADD45? methylation is not one of the common epigenetic changes in PCa. In addition, we suggest that the loss of important regulatory mechanisms involved in GADD45? might play a role in the pathogenesis of BPH.
URI: https://hdl.handle.net/11499/7686
ISSN: 1529-9120
Appears in Collections:Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu

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